Atherosclerosis. Hypertension disease. Symptomatic arterial hypertension презентация

with basis of law




Atherosclerosis (AS) Hypertension disease (HD) Symptomatic arterial hypertension (SAH)






Lecture on pathological anatomy
for the 3-rd year students

the accumulation of cholesterol-rich fat in the intimae of the large and medium-sized arteries of the body.


These masses form plaques

intimae by: cytokines, toxins (exo- and endo-genous), immune complexes...
High blood pressure.
Pathology of lipid exchange at diabetes
mellitus, thyroxin lack.
Law level of muscle activity (lack of
exercise).

Biochemical lesions that promote thrombosis.
Some heredity stations:
Familial combined hyper-lipidemia
Tangier disease.

with resulting increased endothelial permeability or other evidence of endothelial dysfunction.

Increased insudation of lipoprotein, mainly LDL with its high content of cholesterol, and also VLDL.

Cellular interactions in foci of injury involving endothelial cells, monocytes/macrophages, T- lymphocytes, and smooth muscle cells of intimal or medial origin.

Proliferation of smooth muscle cells in the intima with the formation of connective tissue

glycosaminoglycanes. It causes development of edema and fixation of lipoproteins, cholesterol and proteins in intimae. There occurs the destruction of endothelium, elastic and collagen fibres of intima's basal membrane.

Stage of fatty stripes (lipidosis). Fatty stripes appear on intimae due to its lipid infiltration, lipoproteins and proteins fixation. Lipids impregnate intimae and are accumulated in macrophages (foam cell). Elastic membranes become swollen.

Stage of liposclerosis. In the areas of lipidosis, a young connective tissue grows and forms fibrous cap. Macroscopically dense, oval, white formations are observed there.

of fibrous cap with formation of amorphous substance (atheromatous detritus).

Stage of ulceration is characterized by the break of the atheromatosis cap cover and forming of ulcer with small hemorrhage into the plaque.

Stage of atherocalcinosis. Dense and fragile cap is formed due to the cap connective tissue infiltration with calcium.

Morphologenesis

injury with adhesion

of monocytes and platelets.
Migration of monocytes (from the lumen) and smooth muscle cells (from the media) into the

intimae.
Smooth muscle cell proliferation in the intimae.

Well-developed plaque.

The plaque contains amorphous pink material with slit-like "cholesterol clefts" of lipid material. There is overlying recent hemorrhage. Thrombus may form on top of such a plaque

Usually it is not complicated by the thrombosis, thromboembolism and embolism of lower extremities. Development of aortal aneurysm is possible.

Atherosclerosis of coronary arteries of heart
- ischemic heart disease (IHD).

Atherosclerosis of renal arteries leads to atrophy of parenchyma, or infarction. Outcome is atherosclerotic nefro-cirrhosis.

Atherosclerosis of arteries of an intestine is complicated by the thrombosis, leading to gangrene or infarction of bowel.

or brain haemorrhage. Atherosclerosis of carotides leads to acute local ischemia and cerebral softening (infarction)

Atherosclerosis of arteries of extremities, very often this process is located in femoral arteries. The thrombosis with gangrene of lower extremity is possible.

Clinic-anatomic forms of atherosclerosis

B (distal) does not involves the ascending aorta

pressure with progression and presence of crisis. There is damage of elastic type arteries and secondary changers in organs.


Arterial hypertension is defined clinically as

borderline when it riches 140/90 mm Hg.

Blood pressure depends of cardiac output and peripheral resistance (elasticity of the arterial system).

established – such cases are called essential or idiopathic or primary.

The increased peripheral resistance resulting in sustained hypertension may arise from:

Increased sympathetic tone

Increased release of renin and generation of
angiotensin

The presence of vaso-constrictive substances
in the blood circulation

Increased sodium load and extracellular fluid load

A postulated excessive responsiveness to the other factors

may be associated with disturbance of detectable mechanisms – such cases are secondary hypertension. Examples:
Kidney diseases

Hyper-function of adrenal cortex. May be Cushing ‘s syndrome – corticosteroid excess

Tumor of adrenal medulla (pheochromocytoma) – catecholamine excess.

Hypertension occurs in toxemia of pregnancy

elastic structures of arterioles and small-sized arteries, spasm of arterioles. At this stage the hypertrophy of the left ventricle of heart begins.

A stage of general changes of arteries begins as arterial pressure increases. Arteriolar walls permeability is increased, it results in plasmatic impregnation and hyalinosis. Elastic,
muscular-elastic and musculary arteries walls undergo elastofibrosis and atherosclerosis.

in connection with changes of arteries and insufficiency of the intra- organic blood circulation.


Types of hypertension disease:

benign H. - changes develop slowly, that results in atrophy of parenchyma and sclerosis of organ

malignant H. - changes develop quickly (spasm, thrombosis, fibrinoid necrosis) and causing infarctions and hemorrhages.

arteriolosclerosis, which most often appears in the kidney in patients with malignant hypertension. The arteriolar wall is markedly thickened and the lumen is narrowed

Sometimes the small arteries and arterioles can be damaged so severely in malignant hypertension that they demonstrate necrosis with a pink fibrin-like quality that gives this process its name--fibrinoid necrosis

myocardium occurs. Weight of heart reaches 1 kg, thickness of left ventricle walls is up to 3 cm. Heart is called “cor bovin”. Atherosclerosis of coronary arteries of heart is a result of hypoxia of the myocardium, dystrophic and necrobiotic processes.

Cerebral form is characterized as impairment of cerebral blood circulation. Infarctions of the brain and hypooxygenous changes are possible. As the result of brain vessels rupture hemorrhage into tissue can be observed (Hematoma).

by chronic arteriolo-sclerotic nephrosclerosis. Kidney has a term primary shrunken kidney.

In case of malignant hypertension can develop as hypertonic crisis - acute increase of arterial pressure in connection with spasm of arterioles.

Morphological appearance of hypertonic crisis: plasmatic impregnation or fibrinoid necrosis of arteriolar walls.